Related Experiment Video
Updated: May 30, 2026

Closure of a Patent Foramen Ovale (PFO): An Intervention Sequence
Published on: December 23, 2022
Patent foramen ovale and hypercoagulable state in the pathogenesis of acute thrombotic myocardial infarction
Leonarda Galiuto1, Simona Giubilato, Alberto R De Caterina
1Catholic University, Cardiology Institute, 1, L.go F. Vito, Rome, 00168, Italy.
Patent foramen ovale (PFO) is a known cause of cryptogenic stroke and, when associated with a condition of thrombophilia, its closure has been shown to reduce the recurrence of cerebral embolic events. Here we present a case of a young man, with a history of previous recurrent cerebral ischaemic episodes, that developed an inferior acute myocardial infarction (AMI) with angiographic evidence of thrombotic occlusion of the right coronary artery (RCA). Thrombus aspiration followed by balloon angioplasty was performed and, after 24 h of glycoprotein IIb/IIIa inhibitor infusion, thrombus was no longer evident at coronary angiography. Screening for thrombophilia revealed heterozygosis for prothrombin G20210A polymorphism. At transoesophageal echocardiography (TOE), a large PFO with right-to-left atrial shunt was present. Given the history of multiple thrombotic clinical events and the associated state of thrombophilia, transcatheter PFO closure was successfully performed. At 12 months of follow-up the patient was completely asymptomatic.
Patent foramen ovale (PFO) is a known cause of cryptogenic stroke and, when associated with a condition of thrombophilia, its closure has been shown to reduce the recurrence of cerebral embolic events. Here we present a case of a young man, with a history of previous recurrent cerebral ischaemic episodes, that developed an inferior acute myocardial infarction (AMI) with angiographic evidence of thrombotic occlusion of the right coronary artery (RCA). Thrombus aspiration followed by balloon angioplasty was performed and, after 24 h of glycoprotein IIb/IIIa inhibitor infusion, thrombus was no longer evident at coronary angiography. Screening for thrombophilia revealed heterozygosis for prothrombin G20210A polymorphism. At transoesophageal echocardiography (TOE), a large PFO with right-to-left atrial shunt was present. Given the history of multiple thrombotic clinical events and the associated state of thrombophilia, transcatheter PFO closure was successfully performed. At 12 months of follow-up the patient was completely asymptomatic.
Related Concept Videos
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Hemorrhagic Stroke ll: Pathophysiology
Venous Thrombosis I: Introduction
Ischemic Stroke ll: Pathophysiology
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
